Inhibition of Carbonic Anhydrase (CA) on luminal membrane and in the PCT cell--decrased CO2 inside PCT cell--further decrease of CA formation--less intracellular HCO3- and H+ leading to decreases reabsoption of Na+ due to less H+ available for Na/H antiporter.
Na+ w/ H2O, K+ and HCO3- pissed out

effects of carbonic anhydrase inhibitors on renal excretion are self-limiting probably because the resulting metabolic acidosis decreases the filtered load of HCO3– to the point that the uncatalyzed reaction between CO2 and water is sufficient to achieve HCO3– reabsorption

They are absorbed in GI tract and eliminated by filtration and tubular secretion (also hepatic-biliary route)
oral or parenteral (diuresis happens in 30min (oral) to 5 min (IV)

Loop diuretic (specific drugs)

Furosemide (Lasix)
Piretanide
Bumetanide
Torsemide
Ethacrynic Acid

Furosemide

additional-nondiuretic effects

Acutely increase systemic venous capacitance and thereby decrease left ventricular filling pressure. This effect, which may be mediated by prostaglandins and requires intact kidneys, benefits patients with pulmonary edema even before diuresis ensues.

)

Ethacrynic Acid (Ethacrynate)> Furosemide

Loop Diuretic

Side Effects

Abnormalities of fluid and electrolyte balance
Allergies
Alkalosis
Ototoxicity-- manifests as tinnitus, hearing impairment, deafness, vertigo, and a sense of fullness in the ears (Ethacrynic Acid (Ethacrynate)> Furosemide--potentiated by aminoglycosides

Contraindications to the use of loop diuretics include severe Na+ and volume depletion, hypersensitivity to sulfonamides (for sulfonamide-based loop diuretics), and anuria unresponsive to a trial dose of loop diuretic.

Thiazides

Organic acids--are both filtered and secreted

Inhibit Na/Cl cotransporter on the luminal membrane of DCT (bind to Cl site)

Dump Na+, Cl-, K+ and at high doses HCO3- (may also inhibit Carbonic Anhydrase), into the urine
Reduce Ca2+ excretion